HIV invades white blood cells using the trimeric envelope complex (gp160 spike) on the HIV viral envelope, which binds to CD4 receptors, facilitating fusion of the two membranes and entry of the viral RNA genome into host cells. Yet it seemingly must mutate this very protein in order to evade elimination by an antibody response. How can this be accomplished and still maintain high affinity for the CD4 receptor? Is the gp160 spike so large and complex that mutations can occur with enough frequency to allow sufficiently infective virions to be produced which evade immune detection, thereby allowing for its continuous replication despite attempts by the host to eliminate it by repeated antibody responses?
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